Genome- and epigenome-wide analysis of endothelial cell activation and inflammation

DOI 57 References
  • Minami Takashi
    Division of Vascular Biology, RCAST, The University of Tokyo, Tokyo, Japan

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Abstract

Activation and dysfunction of the endothelium underlie many vascular disorders including atherosclerosis, tumor growth, and inflammation. Endothelial cell activation is mediated by many different extracellular signals, which results in overlapping, yet, distinct patterns of gene expression. Comparative ChIP-seqs with either STAT6, GATA2, or NFATc1 antibody between endothelial cells and erythroids or lymphoids revealed that each transcription factor bound the consensus recognition motif genome-widely, but the bound regions showed exclusive cell type specificity and strong correlation to the each cell's crucial function. By using the ChIP-seqs with epigenetic histone modification in endothelium, constitutively expressed GATA2 and chronic IL-4-stimulated STAT6 binding regions were detected at both proximal and distal promoters. In contrast, VEGF-stimulated NFATc1 preferentially bound to the proximal promoters, the majority of which were pre-opened chromatin due to responding to the acute VEGF activation signal. This review is to combine our recent genome/ epigenome wide ChIP-seqs information and the related literatures as well as to summarize the crucial roles of tight regulation by the endothelial cell activation that is pathologically leading to tumor growth and inflammation.

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